This is the more common type of breath-holding spell. The spell usually begins with uncontrolled crying that follows a seemingly trivial event, such as being reprimanded or sustaining a fall with a head bump. After few seconds of crying, the child holds his or her breath, and cyanosis
develops. At times, consciousness may be lost. Tonic, clonic, or myoclonic movements may occur later in the attack, but are usually self-limited. These involuntary tonic or tonic-clonic movements are secondary to brain hypoxia and should not be treated with anticonvulsants. The interictal EEG is usually normal but may reveal slowing or suppression during the acute event. Aside from the safety issue of a possible fall during a breath-holding spell, these events are considered benign. In some instances, psychologic referral for behavior modification is required and may benefit both the parents and the child. In most instances, children outgrow breath-holding spells without sequelae or future behavioral problems. The pathophysiologic mechanism is not well understood, but correction of any underlying anemia has been shown to reduce the frequency of attacks, with reports suggesting iron therapy even without frank anemia can be helpful.

In the pallid type of spell, bradycardia or brief asystole causes a loss of consciousness soon after the attack begins. Again, the attack may be precipitated by a head bump that may be seemingly trivial. The child suddenly becomes pale and often loses consciousness. Clonic or myoclonic jerks may occur near or at the end of the attack. Most patients suspected of having this syndrome may undergo routine ECG and Holter monitoring to exclude any treatable cardiac condition or rhythm disorder. Children with pallid breath-holding spells are believed to have autonomic dysregulation caused by parasympathetic disturbance distinct from that found in cyanotic breath-holding. In severe cases, atropine or similar agents may be used to block the bradycardia associated with the syndrome.

Gastroesophageal reflux in children, usually infants, sometimes presents with unusual posturing of the neck, torso, and arms. The posturing may be sustained (like dystonia) or intermittent. It may also present as apneic episodes with cyanosis and or pallor. This disorder is most often described in children with tone abnormalities and developmental disorders, but may occur in normal children. The diagnosis is confirmed with a pH probe test. Episodes usually resolve with treatment of gastroesophageal reflux.

Cyclic vomiting is characterized by spontaneously recurrent bouts of severe emesis lasting minutes to many hours. In some cases the emesis can last for several days before relenting. The cycles of emesis occur every few weeks to months. The episodes may be precipitated by stress, infection, fasting, poor sleep, or mesntrual periods. No cause is apparent when the child is investigated during an acute episode. A diagnosis of viral gastritis or gastroenteritis is usually presumed during initial episodes before the correct diagnosis is recognized. The child is normal between episodes, and the examination findings raise no concerns. Cyclic vomiting is usually seen in young children. The syndrome has also been considered a migraine variant, as it has been shown occasionally to evolve into migraine headaches. In some children, the family history is also positive for migraine. If the patient has experienced many episodes over time, the physician may be able to make the diagnosis without the use of laboratory tests. Defects in intermediary metabolism (including but not limited to urea cycle disorders such as ornithine transcarbamylase deficiency in girls) and intracranial pathology may present with recurrent vomiting, and these should be considered in appropriate clinical scenarios. Acute episodes may require intravenous hydration, antiemetics, and mild sedation. Triptans may be used in the acute treatment when headache is a prominent symptom. Prophylactic treatment of cyclic vomiting may require antimigraine medications such as cyproheptadine, β-blockers, and tricyclic antidepressents. Topiramate, valproate, and calcium channel blockers, used widely in migraine prophylaxis, are other agents that have been anecdotally reported to be effective in cyclic vomiting.

Benign neonatal myoclonus is a common condition seen in newborns and young infants. It is seen during sleep as rapid (myoclonic) movements involving one or more extremities or the torso in a random fashion. The movements occur as isolated events or in intermittent clusters that may continue during all stages of sleep. Attacks are usually a few minutes in duration, but in some infants movements may last for hours, intruding into sleep. Passive restraint of extremities does not stop the movements. EEG shows no epileptiform activity during the movements. The movements stop when the infant is woken up and are never seen in a fully awake and alert baby. No treatment is generally required. The movements typically disappear over several months. It is important to recognize this benign condition as it may lead to overaggressive investigation and treatment looking for seziures resulting from genetic or metabolic causes. Infants with this condition have had brain MRIs, cerebrospinal fluid examinations, skin and muscle biopsies, and admission to the intensive care unit with intravenous regimens of mulitiple antiepileptic medications.

This disorder is considered a form of parasomnia usually seen during the periods of transition from wakefulness to sleep or between different stages of sleep. Onset is usually in infancy. The child performs bizarre head and neck movements, such as head banging or rolling. Events may last from 15 to 30 minutes. Soon the child drifts off to sleep and the movements disappear. Episodes rarely recur in the same night during periods of sleep transition. The EEG is usually normal both during and between the episodes. Most children recover within few years after onset. Many parents have to repeatedly check the child at night when they wake up from the sounds of head banging. Parental reassurance is necessary. Measures to ensure safety (from fall or head banging against hard objects) of the child in his or her bed at night are important. Rarely, short-acting benzodiazpenes may be used half an hour before bedtime with good results.

Nightmares are behavior episodes that are believed to be associated with sleep dreams. They occur during REM sleep. Onset may be at any time, but is usually at around 2 to 5 years of age. Children may spontaneously wake up and be restless, crying, frightened, and sometimes have autonomic symptoms. They cling to the parents and generally calm down when reassured. Occasionally, incontinence may occur during a frightening episode, which may lead to a misdiagnosis of seizure. Most children are able to at least partially recall the dream. An EEG recorded during these events shows arousal from REM sleep. Most children improve over the course of few years. Episodes are generally infrequent and lead to no significant sleep disruption. Most children warrant no treatment. Counseling may help in older children with frequent episodes who are afraid to go to bed alone at night.

Night terrors are considered to parasomnias that occur during the deep stages of non-REM sleep (stages III and IV). They usually begin around the age of 4 to 8 years, slightly later than the age of onset for nightmares. The child suddenly wakes up with inconsolable screaming, profuse sweating, agitation, tachycardia, and dilated pupils. The attack lasts for several minutes, and may even continue for as long as 15 to 20 minutes. It is often difficult to console or reason with the child during an episode. The child usually drifts back to sleep once the attack is over. Most children are not able to recall the episode the next morning. Attacks are usually isolated events a few nights a month, causing no regular sleep disruption. The usual course is that of improvement and subsequent disappearance of episodes. The parents usually are very apprehensive, and may demand confirmation by video EEG for reassurance. No treatment is generally recommended.

Sleepwalking is an uncommon type of parasomnias that occurs during the deep stages of non-REM sleep (stages III and IV). The usual age of onset is 5 to 12 years. The child gets up from the bed, usually mumbling with a vacant look and open eyes, and then walks around in a trance before returning to bed. The usual time of occurrence is 2 to 4 hours after falling asleep. Sometimes bizarre activities such as eating, dressing, opening doors and windows, and touching objects are seen during an episode of somnambulism. The child rarely walks into objects. Most children sleepwalk close to their bed and the room in which they were sleeping. Episodes may last for several minutes, and never occur more than once in a night. Children are unable to recall the episodes the next morning. Serious accidents are rare in sleepwalking children. Violence is not described during typical events. Most children are able to be calmly redirected to their bed when parents find them during an episode. Complex partial seizures should be excluded before a diagnosis of sleepwalking is presumed. Treatment usually is not necessary if the child’s safety can be ensured at night. Short-acting benzodiazepines are sometimes indicated for frequent or prolonged attacks of sonambulism.

These are rare sleep disorders, but are important differential diagnoses in children who suddenly lose tone and posture. Narcolepsy is sudden intrusion of REM sleep during wakefulness, leading to excessive daytime sleepiness. Other symptom complexes in patients with narcolepsy include sleep paralysis (transient episodes of inability to move on awakening), hypnagogic hallucinations, and cataplexy. Cataplexy produces a sudden loss of tone with a drop to the ground in response to an unexpected touch or emotional stimulus, such as laughter. Children with narcolepsy and cataplexy may present with attention difficulties in school, irritability, and unexplained fatigue and falls. Consciousness is not lost during these brief attacks. Narcoleptics have short sleep latency as measured by standardized measurement of sleep latency tests (MSLT). MSLT will show REM sleep patterns on EEG recordings within 10 minutes of falling asleep. It is important to demonstrate normal sleep the night before an MLST with a polysomnogram (PSG), as primary sleep disorders such as sleep apnea syndrome can cause a narcoleptic picture, when in fact the patient is not sleeping at night and thus is excessively tired during the day. Narcolepsy is strongly associated with the HLA DQB1*0602 genotype, and is also associated with HLA DR2 and HLA DQ1, but narcolepsy is multifactorial and these tests are not diagnostic.
Narcolepsy may be treated with a stimulant drug, but behavioral management is also important as part of the comprehensive treatment plan.

Acute confusional migraines begin with an acute alteration in consciousness, which may include varying degrees of lethargy, disorientation, agitation, and stupor. Fugue-like states are also described. Abnormal behaviors may be intermittent with somnolence, alternating with agitation and inappropriate motor hyperactivity. Episodes of acute confusional migraine typically last for a few hours, much longer than a complex partial seizure. These events may not be accompanied by any headache as in classic migraine. Patients frequently sleep for a few hours after an episode is over. When questioned later, patients are generally not able to completely recall the episode. Acute confusional migraine begins in childhood, after the age of 5 years, and may eventually evolve into typical migraine as the patient becomes older. A positive family history of migraine is usually present, and is very useful for making a diagnosis. The differential diagnosis includes a prolonged partial complex seizure, nonconvulsive status epilepticus, drug intoxication, and other etiologies that cause acute encephalopathy. If the diagnosis reamains unclear, a video EEG is helpful in distinguishing this disorder from a seizure. Acute episode is treated with ensuring safety, intravenous hydration, sedation (induce sleep), and control of emesis and pain (if headache is present). The role of tryptans is controversial: the management of acute confusional migraine. Prophylactic antimigraine therapy may be helpful in preventing frequent and prolonged attacks but no class I data are currently available.